Micro-nanoplastics and human health

Micro/nanoplastics (MNPs) are plastic particles smaller than 5 mm in diameter, classified into microplastics (1 μm–5 mm) and nanoplastics (<1 μm). These particles originate from diverse sources, including the degradation of larger plastic waste due to environmental factors such as UV radiation, mechanical abrasion, and chemical weathering. Additionally, MNPs are intentionally manufactured for use in various products, such as plastic microbeads in personal care items, synthetic fibers from textiles, and additives in industrial processes. The most common types of MNPs include polyethylene (PE), polystyrene (PS), polycarbonate, polypropylene (PP), and polyethylene terephthalate (PET), materials widely used in packaging, consumer goods, and industrial applications. Due to their small size and persistence, these particles are found in air, water, soil, and food products, raising concerns about their accumulation in ecosystems and potential health risks to humans (Table 1). ^{Reference Lin8}

Table 1.

Common chemicals found in micro/nanoplastics

The global proliferation of plastic products and their improper disposal have led to the widespread contamination of ecosystems by MNPs, making them a pressing environmental concern. During their lifecycle—manufacturing, usage, and disposal—plastics release vast quantities of microscopic particles through physical abrasion, chemical degradation, and environmental weathering. Due to their highly stable chemical composition, these plastic fragments resist natural decomposition, persisting in the environment for extended periods. Their minute size enables them to be easily transported by air and water currents, facilitating their dispersal across diverse ecosystems. As a result, MNPs have been detected in remote regions, including deep-sea sediments, polar ice, freshwater bodies, agricultural soils, and even atmospheric fallout, underscoring their extensive environmental reach. ⁹ In the ocean, micro/nanoplastics have even been found in deep-sea sediments, ^{Reference Peng, Chen, Chen, Dasgupta and Bai10} demonstrating the extent and depth of their spread and pollution.

The presence of MNPs poses a serious threat not only to the ecological environment but also to human health, as they can enter the food chain and water supply system through various pathways, leading to the absorption and bioaccumulation of MNPs in the human body, ultimately impacting human health. For example, marine organisms may ingest microplastics, introducing them into the food chain. Humans may ingest MNPs by consuming contaminated seafood, aquatic products, and drinking water. Once inside the human body, MNPs can potentially cause tissue damage and functional disorders in multiple systems (such as the digestive, respiratory, cardiovascular, immune, reproductive, and endocrine systems) through mechanisms such as cellular damage, inflammatory responses, metabolic disorders, genotoxicity, and immune and endocrine disruption, thereby posing potential health risks. ^{Reference Zhao11}

Additionally, MNPs can act as carriers, carrying and adsorbing numerous harmful substances such as chemical additives, environmental pollutants, and pathogenic microorganisms. These attached harmful substances can enter the human body through the food chain along with the MNPs, increasing health risks and potentially affecting future generations(Figure 1). ^{Reference Blackburn and Green12}

Figure 1.

Micro/nanoplastics pollution sources, entry routes and effects on intrauterine development and growth.

Microplastics detection technologies

Recently, scientific research on microplastics has been booming, and the precise and rapid identification of microplastics is crucial for research in this field. Depending on the type, size, color, abundance, and weight of microplastics, the main detection methods include but are not limited to optical microscopy, scanning electron microscopy (SEM), Fourier-transform infrared spectroscopy (FTIR), Raman spectroscopy, pyrolysis-gas chromatography-mass spectrometry (Py-GC-MS), thermal extraction-desorption gas chromatography-mass spectrometry (TED-GC-MS), and thermogravimetric analysis-differential scanning calorimetry (TGA-DSC). ^{Reference Lee and Chae13,Reference Ahmed14}

Detection of micro/nanoplastics in human tissues

Micro/nanoplastics are widely present in the human body through skin contact, respiratory inhalation, and digestive ingestion. Using a 3D human skin model, a recent study found that toxic chemicals contained in microplastics can penetrate the skin through contact with sweat and then enter the bloodstream. ^{Reference Abafe, Harrad and Abdallah30} Microplastics not only are present in the air but can also enter the lungs through respiration. A systematic review found that inhaled microplastics might cause inflammatory responses and potential carcinogenic effects in the respiratory system, varying with the concentration, size, type, and surface charge of the microplastics. Accumulation of microplastics in the lungs may lead to chronic inflammation, tissue damage, and pulmonary diseases, especially with long-term exposure. ^{Reference Lombardi31} Most micro/nanoplastics ingested through diet and drinking water may be excreted through feces. Some studies suggest that over 90% of micro/nanoplastics are not absorbed into the body; however, small particles, especially those smaller than 10 μm, can be absorbed by intestinal cells through processes such as phagocytosis and endocytosis. ^{Reference Udovicki, Andjelkovic, Cirkovic-Velickovic and Rajkovic32}

In recent years, multiple studies have confirmed the widespread presence of microplastics in the human body, but these findings have not been definitively confirmed. These studies have revealed that microplastics not only accumulate in various organs and tissues but are also present in various bodily fluids and secretions (Table 2). Research indicates that microplastics can enter the circulatory system. ^{Reference Leslie33} In the blood, these tiny particles can be transported to organs such as the liver, ^{Reference Horvatits34} kidneys, ^{Reference Massardo23} heart, ^{Reference Liu35} and intestines, ^{Reference Ibrahim36} reaching the testes, ^{Reference Zhao37,Reference Yang38} endometrium, ^{Reference Sun39} lower limb joints, ^{Reference Li18} and even depositing on the arterial walls, ^{Reference Liu28} forming components of thrombi. ^{Reference Liu28} Inhaled microplastics can accumulate in the lungs, causing inflammation and tissue damage. ^{Reference Amato-Lourenço40,Reference Jenner41} Additionally, microplastics have been detected in human semen ^{Reference Montano42} and urine, ^{Reference Song17} indicating potential impacts on the male reproductive and urinary systems. The detection of microplastics in respiratory secretions such as sputum further confirms their inhalation through the respiratory tract. ^{Reference Huang43} The presence of microplastics in feces indicates that these particles are ingested and excreted through the digestive system. ^{Reference Yan44} Microplastics found in the placenta, ^{Reference Ragusa5} breast milk, ^{Reference Liu35} and amniotic fluid ^{Reference Xue7} suggest that microplastics in the mother’s body can be transmitted to the infant, posing potential risks to the health of newborns even before birth.

Table 2.

Toxic effects of microplastics

Effects of MNPs on offspring growth and development in animals

Pregnancy and lactation are vulnerable periods of vulnerability to the harmful effects of environmental exposures. However, the adverse effects of maternal exposure to MNPs on fetal health are largely unknown. Studies have shown that micro/nanoplastics ≤ 20 μm can enter organs, and smaller MNPs with a particle size of 0.1–10 μm can penetrate all organs of animals; cross cell membranes, the blood-brain barrier, and the placenta; and even transfer to the next generation. ^{Reference Wright and Kelly45,Reference Bouwmeester, Hollman and Peters46} For example, when adult zebrafish are exposed to PS nanoplastics, these microplastics bioaccumulate and are inherited by the offspring. Nanoplastics have been found in the yolk sac, gastrointestinal tract, liver, and pancreas of embryo/offspring zebrafish, with bradycardia observed in embryos. ^{Reference Pitt47} Numerous animal experiments have demonstrated that maternal exposure to MNPs profoundly affects offspring growth and development, including weight loss, developmental abnormalities, immune disorders, metabolic disturbances, circulatory system abnormalities, neurological deficits, and reproductive failure. ^{Reference Geng48}

In vivo studies have shown that 24 hours after Sprague Dawley rats inhale PS nanoplastics during pregnancy, nanoplastics can be transmitted from the mother to the fetus. PS nanoparticles have also been observed in the placenta, as well as in the liver, lungs, heart, kidneys, and brain of fetal rats. The weight of the fetuses and placentas was significantly lower than that of the control group. ^{Reference Fournier49} Exposure to PS MNPs during pregnancy and lactation in mother mice can lead to reduced birth weight and postnatal weight in offspring. Similar findings were observed in three other studies. ^{Reference Zhang50} In oyster embryos exposed to high-density PE microplastics of different sizes for 24 hours, smaller microplastic particles induced higher rates of deformities and developmental stasis in the oysters. ^{Reference Bringer51} Another study exposed oysters (Crassostrea gigas) to a mixture of microplastics and found reduced activity, developmental abnormalities, growth stasis, and delayed development in the offspring. ^{Reference Bringer52} Zebrafish embryos exposed to microplastics showed developmental disorders, including significant growth retardation and peripheral microcirculation disorders, leading to premature birth and growth restriction during embryonic development. ^{Reference Park and Kim53} Additionally, offspring of zebrafish exposed to microplastics during pregnancy showed bone formation disorders at 6 days old, manifesting as reduced operculum bone. ^{Reference Tarasco54} Juvenile zebrafish exposed to microplastics exhibited severe developmental deformities and impaired integrity of the eye’s visual structure during development. ^{Reference Marco De55} PS nanoplastics can cause extensive severe congenital malformations in chick embryos, particularly leading to severe defects in the heart and major blood vessels. ^{Reference Wang56}

An increasing number of animal experiments has demonstrated that MNPs exposure affects offspring through the immune system. Zebrafish embryos exposed to PS microplastic particles can trigger an immune response, activating several biological pathways related to immune response. Neutrophils and macrophages are recruited around the microplastic particles, indicating that plastic particles are involved in the immune recognition process. ^{Reference Veneman, Spaink, Brun, Bosker and Vijver57} PS microplastics can disrupt the maternal-fetal immune balance, shifting cytokine secretion towards an immunosuppressive state, reducing the number and diameter of uterine arterioles, leading to embryo resorption in mice, and inducing natural miscarriages. This finding suggests that PS microplastics can adversely affect pregnancy outcomes through immune dysregulation. ^{Reference Hu3}

MNPs exposure can adversely affect the circulatory and metabolic functions of offspring. Numerous studies have demonstrated that maternal exposure to PS microplastics can disrupt various organ functions in offspring by altering their metabolism. For instance, it can alter serum metabolite levels and increase the risk of fatty acid metabolism disorders, potentially influenced by the particle size of the microplastics. ^{Reference Luo58} Additionally, it can cause maternal metabolic disorders associated with gut microbiota imbalances and intestinal barrier dysfunction, heightening the risk of long-term metabolic issues in offspring. MNPs may also disrupt amino acid metabolism in the retina of offspring and lead to fetal growth restriction (FGR) and intrauterine death by affecting maternal hepatic glucose metabolism. ^{Reference Xiong4,Reference Zhang50}

Maternal exposure to PS nanoplastics can result in abnormal brain metabolism in mouse fetuses, with significant reductions in the relative concentrations of γ-aminobutyric acid (GABA), creatine, and glucose compared to controls. ^{Reference So59} Experimental animal studies have shown that maternal exposure to microplastics environments can alter offspring energy and lipid metabolism, potentially leading to obesity. ^{Reference Kannan and Vimalkumar60} Zebrafish studies have indicated that exposure to PS MNPs can significantly alter the metabolic profiles of juvenile fish, affecting genes related to glycolysis and lipid metabolism, and may cause pericardial edema. Micro/nanoplastics may induce systemic inflammatory responses and oxidative stress, resulting in vascular cell dysfunction, endothelial dysfunction, and thrombosis. ^{Reference Wan61,Reference Sun62}

MNPs also impact neural development in offspring. Recent studies show that PS plastics during pregnancy can cause placental dysfunction in mice, significantly reducing the pulsatility index of the middle cerebral artery in fetuses and potentially leading to neurodevelopmental disorders. ^{Reference Dibbon63} PS nanoplastics ingested by pregnant mice can be transmitted to offspring through breast milk, altering neural stem cell function, neural cell composition, and brain histology, resulting in neuronal dysfunction and cognitive deficits. ^{Reference Jeong64} In another study, pregnant mice exposed to PS microbeads exhibited thalamic neuronal apoptosis and reduced GABA synthesis in fetal mice, leading to anxiety-like behavior at 8 weeks. ^{Reference Yang65} Additionally, maternal exposure to PE microplastics produced offspring with autism-like traits, including repetitive and compulsive behaviors. ^{Reference Zaheer66} Long-term exposure to PS microplastics has been linked to increased proliferation and apoptosis of primary cortical neuronal cells, potential neurotoxic effects, impaired social novelty preference, and anxiety-like behavior in adolescent offspring. ^{Reference So59} Exposing mother mice to PS nanoplastics during late pregnancy, late lactation, and adolescence resulted in altered brain neurotransmitter levels and hippocampal synaptic changes, ultimately leading to anxiety-like behavior and spatial memory deficits in adolescent offspring. This finding demonstrates that maternal exposure to microplastics affects the neurodevelopment of offspring. ^{Reference Tian67} Exposure to PS nanoplastics during pregnancy in rats leads to oligodendrocyte apoptosis and impaired motor coordination in offspring, affecting the brain development of fetal rats. ^{Reference Zhang68} Research also found that PS microplastics inhibit chicken embryo development and increase the incidence of congenital malformations (especially in the nervous system), including neural tube defects. ^{Reference Nie69}

Animal experiments suggest that microplastic exposure during pregnancy can disrupt offspring fertility. Maternal exposure to PS nanoplastics has been shown to cause liver and testicular toxicity in male offspring, inducing oxidative damage and testicular developmental disorders. In Daphnia magna, microplastic exposure increased parental mortality and reduced growth, reproduction, and population growth rates, with effects persisting into subsequent generations. PS microplastic exposure led to decreased mortality and reproductive rates in earthworms, likely due to DNA damage. ^{Reference Martins and Guilhermino70,Reference Sobhani, Panneerselvan, Fang, Naidu and Megharaj71} Pregnant mice and their offspring exposed to PS microplastics from day 1 of pregnancy to after birth experienced testicular developmental disorders and impaired male fertility, potentially regulated by the Hippo signaling pathway and involving an immune response. This response may be regulated by the Hippo signaling pathway and involve an immune response. ^{Reference Zhao72} Overall, animal studies support the notion that exposure to micro/nanoplastics during pregnancy adversely affects the growth and development of offspring.

MNPs and pregnancy-related diseases

Studies have found that MNPs particles can cross the placental barrier in various experimental models, ^{Reference Medley, Spratlen, Yan, Herbstman and Deyssenroth73} including in vitro cell models, ^{Reference Cartwright74} in vivo animal models, ^{Reference Fournier49} and ex vivo human placental perfusion systems. ^{Reference Wick75} This finding provides evidence of the potential impact of maternal MNPs on the fetus through the maternal-fetal barrier. A study using Raman spectroscopy detected microplastic contamination in placentas during pregnancies in Hawaii in 2006, 2013, and 2021. The results showed that the accumulation of microplastics in placentas significantly increased over time. ^{Reference Weingrill76}

However, direct evidence confirming the association between human MNPs exposure during pregnancy and pregnancy-related diseases remains scarce. One study analyzed the relationship between microplastics and neonatal growth and development, finding a significant negative correlation between the amount of microplastics in the placenta and neonatal birth weight, length, head circumference, and 1-minute APGAR score in pregnancies complicated by intrauterine growth restriction (IUGR) (r = −0.82, p <0.001). All placentas from IUGR pregnancies contained microplastic particles, whereas only four of 30 placentas from normal pregnancies contained microplastic particles. According to the study, the most prevalent microplastics were PE and PS. Although the sample size of this study was small (13 cases), it draws attention to the potential impact of microplastic particles on fetal development in utero. ^{Reference Amereh77} A study using experimental mice to test the effects of maternal exposure to plastics on fetal and placental growth found that exposure to microplastics in late pregnancy resulted in FGR. ^{Reference Jeong64} Researchers further explored the reasons in another study, confirming that this phenomenon may be due to altered placental metabolism. ^{Reference Xiong4} Additionally, the latest research explores the association between microplastic levels in maternal amniotic fluid and fetal growth indicators. The results indicate a significant negative correlation between the abundance of total microplastics in maternal amniotic fluid and gestational age (β = −0.44, 95% CI, −0.83, −0.05), suggesting that maternal microplastic exposure may have potential health impacts on fetal development. ^{Reference Xue7}

Studies investigating the relationship between unexplained recurrent miscarriage (RM) and MNPs documented higher levels of PS in the villous tissue of RM patients. Additionally, this study utilized human placental trophoblast cells and pregnant mouse models to confirm that exposure to PS nanoplastics activates the Bcl-2/Cleaved-caspase-2/Cleaved-caspase-3 signaling pathway through the mitochondrial pathway, leading to excessive apoptosis in human trophoblast cells and mouse placental tissue, further inducing miscarriage. ^{Reference Wan78}

A substantial number of animal experiments also support the link between maternal MNPs exposure and pregnancy-related diseases. South Korean researchers studied the effects of polymethyl methacrylate (PMMA) nanoplastics on mouse embryo development and found that PMMA particles reduced blastocyst development and embryo quality indicators and decreased the implantation rate of morulae. ^{Reference You79} PS microplastics have been shown to disrupt hepatic glucose metabolism in pregnant mice, induce insulin resistance, and damage placental structure, leading to FGR and intrauterine death in the offspring. ^{Reference Zhang50}

Additionally, multiple studies have reported that PS MNPs can result in reduced fetal weight ^{Reference Dümichen1,Reference Abafe, Harrad and Abdallah30,Reference Zhao37,Reference Yang38,Reference Wan61,Reference Amereh77} and cause developmental deformities in Crassostrea gigas and developmental delays and extensive malformations in chick embryos. ^{Reference Dümichen1,Reference Abafe, Harrad and Abdallah30,Reference Zhao37,Reference Yang38,Reference Wan61,Reference Amereh77} In studies related to zebrafish, PS microplastics were found to cause premature birth and growth restriction in juvenile fish, as well as developmental deformities. ^{Reference Park and Kim53–Reference Marco De55}

PS nanoplastics may inhibit the invasion and migration of human trophoblast cells by activating autophagy, promoting the autophagic degradation of SOX2, and suppressing the transcription of ROCK1, thereby inducing miscarriage in pregnant mice. ^{Reference Wan80} Additionally, they may disrupt the maternal-fetal immune balance, shifting cytokine secretion towards an immunosuppressive state, reducing the number and diameter of uterine microarteries, and leading to spontaneous miscarriage. ^{Reference Hu3} These findings are consistent with previous research conclusions. ^{Reference Wan78}

Another study, which experimented with exposure to PE MNPs in mice showed that although maternal exposure to PE does not affect fetal growth, the umbilical artery blood flow in the PE group increased by 43% compared to the control group, significantly impacting placental function (p < 0.01). These findings suggest that PE could potentially lead to adverse pregnancy outcomes through abnormal placental function. ^{Reference Xiong4,Reference Luo58,Reference So59}